Speaker Profile

Executive Summary：
Dr. Phil Hyu Lee graduated from College of Medicine, Yonsei University, and received PhD training from the same University, He received his neurological residency training in Severance Hospital.
Dr. Lee is now a professor in Department of Neurology and Severance Biomedical Science Institute, Yonsei University. His main academic interests are translational research on alpha-synuclein modulation and Parkinson’s disease and multiple system atrophy and neuroimaging studies in patients with PD and dementia with Lewy bodies. He has published about 200 papers in the field of movement disorders as a main author.
He has played an important role in Korean Movement Disorder Society (KMDS) and is now the president of KMDS.

Lecture Abstract：
Multiple system atrophy (MSA) is a sporadic neurodegenerative disease of the central and autonomic nervous systems. Clinically, MSA is characterized by autonomic dysfunction, parkinsonism, cerebellar ataxia, and pyramidal signs, in which autonomic dysfunction is an integral component. Pathologically, MSA is characterized by α-synuclein- positive glial cytoplasmic inclusions. Initially, by unknown etiology, expression of alpha-syn is increased in oligodendrocytes. In addition with environmental factors, mitochondrial dysfunction and oxidative stress may lead to increased cell-to-cell propagation and accumulation of alpha-synuclein. Taken together, dysfunction in clearing cellular systems and neuroinflammation may further deteriorate the neurodegenerative processes. Many clinical trials have been performed in patients with MSA, however, these trials have been failed and currently, there are no symptomatic or disease-modifying therapeutics in MSA patients.
The benefit of repurposing strategies is bypassing the need for preclinical safety testing and formulation optimization, thereby saving both time and costs involved in getting a treatment to the clinic. Also, reduced failure rates for repurposed drugs are potentially benefit. Here, I summarize some repositioning drugs that were previously reported in the field of MSA. As well, I introduce possible candidates of repositioning therapeutics in patients with MSA based on our experience.

Executive Summary：
Tim Anderson, Neurologist, is the Cas Van Der Veer Chair in Parkinson’s and Movement Disorders at the Department of Medicine, University of Otago, Christchurch and Clinical Director of the New Zealand Brain Research Institute (NZBRI) in Christchurch. He is co-director of the Christchurch Dementia Prevention Research clinic. His clinical interests are in Movements Disorders, especially Parkinson’s and Huntington’s disease, dementia, and eye movements . Research interests are in biomarkers of cognitive impairment and progression in Parkinson’s disease, as well as many other aspects of Parkinson’s – advanced brain imaging (MRI and PET), EEG, epidemiology, genetics, behavioural and other non-motor features. Prof Anderson has been active at the committee level in the International Parkinsonism and Movement Disorders Society.

Lecture Abstract：
The careful clinical examination of eye movements can be a useful adjunct in the diagnosis of many movement disorders. Laboratory eye movement recordings do not usually provide additional diagnostic clues but show promise as biomarkers for disease monitoring and measuring treatment response in trials of novel therapeutics. Future work is still needed to explore the robustness and repeatability of laboratory eye movement recordings in healthy controls and disease states. As a general rule, the clinical examination of saccades yields the greatest reward in clinical diagnosis. Atypical parkinsonian disorders are associated with distinctive features; slowed saccades in PSP, positional and head-shaking downbeat nystagmus in multiple system atrophy, and saccadic apraxia in corticobasal syndrome. Oculomotor hallmarks that aid in diagnosis of other disorders are slowed saccades, encountered in a number of genetic and non-genetic movement disorders, including spinocerebellar ataxia (SCAs 1,2 and 7), Huntington’s disease, anti-IgGLON5 disease and others. CANVAS has characteristic eye movement changes reflecting the combination of vestibular failure and cerebellar dysfunction. Movement disorders related to anti-neuronal antibodies can be associated with a range of oculomotor features. The presentation will be illustrated by videos, and include tips in the bedside oculomotor examination, examples of frequently encountered abnormal signs, and cover a range of movement disorders associated with eye movement changes.

Executive Summary：
Pramod Kumar Pal, MD, DNB, DM, FIAN, FRCP (Lon)
Dr. Pramod Kumar Pal is working as Professor of Neurology and program director of the post-doctoral Fellowship Program in Movement Disorders at the National Institute of Mental Health & Neurosciences (NIMHANS), Bengaluru, India. After obtaining MBBS, MD (Medicine) and DM (Neurology) degrees from India, he did fellowship in Movement Disorders at Vancouver and Human Motor Physiology at Toronto. His areas of interest include Parkinson’s Disease, ataxias, hyperkinetic movement disorders, rare movement disorders, genetics and Human Motor physiology including Transcranial Magnetic Stimulation. He has more than 500 publications.

Currently Dr. Pal is the Chair of the Education Committee of the International Parkinson and Movement Disorder Society (MDS), Chair of Infection Related Movement Disorders Study Group and President-Elect of the Movement Disorders Society of India (MDSI).

Dr. Pal is the Founding Secretary of Movement Disorders Society of India (MDSI) and in the past served as the Treasurer and President of Indian Academy of Neurology, Secretary of MDS-AOS, President of the Parkinson Disease Society of Karnataka and Editor-in-Chief of Annals of Movement Disorders. He also serves as member of the Parkinson’s Research Alliance of India, Rare Movement Disorders Consortium of India, Rating Scales Education and Training Program Committee of MDS, and of several Study Groups of MDS including Rare Movement Disorders, Ataxia, Neurophysiology, Movement Disorders in Asia and Post-Stroke Movement Disorder.

Dr. Pal is a Fellow of the International Association of Parkinsonism and Related Disorders. He is currently working on the formation of a National Parkinson Network (NPN) under the aegis of the Movement Disorders Society of India and has been elected for the award of Lifetime Honorary Membership of IPMDS for his extraordinary contributions in the field of Movement Disorders and to the Society.

Lecture Abstract：
Cerebellar Syndromes induced by Treatable Causes: Diagnosis not to miss

Abstract:

While there is no specific treatment for most of the cerebellar ataxias, there are some cerebellar ataxias which can be treatable. These disorders are referred to “Treatable ataxias” and include rare genetic and metabolic disorders, immune-mediated ataxic disorders, ataxic disorders associated with infectious and parainfectious etiology, vascular causes, toxins and chemicals, and endocrinopathies. My talk will provide a comprehensive overview of different treatable ataxias.

There are several potentially treatable metabolic and genetic disorders which have ataxia with or without other neurologic and systemic manifestations, These include ataxia with vitamin E deficiency, abetalipoproteinemia, cerebrotendinous xanthomatosis, Niemann-Pick disease type C, autosomal recessive cerebellar ataxia due to coenzyme Q10 deficiency, glucose transporter type 1 deficiency, and episodic ataxia type 2. The treatment of these disorders includes the replacement of deficient cofactors and vitamins, dietary modifications, and other specific treatments.

There are a group of immune-mediated disorders which can have ataxia as one of the important manifestations. The treatment of the underlying causes potentially improve ataxia. The treatable ataxias with immune-mediated etiologies include gluten ataxia, steroid-responsive encephalopathy associated with autoimmune thyroiditis, anti-GAD antibody-associated ataxia, Miller-Fisher syndrome, multiple sclerosis, and paraneoplastic cerebellar degeneration. Gluten ataxia can be treated by dietary modification with a gluten-free diet. Other autoimmune ataxias are managed by short-course steroids, plasma exchange, or immunomodulation. In patients with autoimmune ataxias secondary to malignancy, treatment of malignancy can reduce ataxic symptoms.

Potentially preventable and treatable ataxias include those resulting from chronic use of alcohol, heavy metals, exposure to insecticides, antiepileptics, anticancer drugs and recreational drugs. Infective and parainfectious causes of cerebellar ataxias include acute cerebellitis, post-infectious ataxia, Whipple’s disease, meningoencephalitis, and progressive multifocal leukoencephalopathy. These disorders are treated with steroids and antibiotics.

To conclude, every attempt should be made not to miss treatable ataxias. This is important because the timing of treatment can make a significant difference in the course of the disease and symptom reversal.